Related Experiment Video
Updated: Aug 14, 2026

Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature
Published on: April 1, 2014
Fatal meningococcal septicemia
Abstract:
The morphologic and clinical findings in seven fatal cases of meningococcal septicemia are described and interpreted in light of recent experimental and clinical studies. We include evidence that suggests the disease has two distinct pathogenetic mechanisms. First, a shock-like terminal phase is associated with the development of widespread pulmonary microvascular thrombosis. These thrombi, composed largely of platelets and leukocytes, produce severe cor pulmonale that cannot be prevented with heparin sodium treatment. Meningococcal endotoxin also produces disseminated intravascular coagulation, which includes the rapid consumption of fibrinogen and the formation of fibrin thrombi in adrenal and renal glomerular capillaries, causing hemorrhagic infarction of the adrenal glands and renal cortical necrosis. This secondary phase of the disease can be modified with heparin therapy, but its control does not improve survival because the parenchymal lesions produced are not immediately life threatening.
Insights
Meningococcal septicemia involves two main processes: pulmonary microvascular thrombosis causing cor pulmonale and disseminated intravascular coagulation leading to organ damage. Neither heparin nor current treatments fully prevent these severe outcomes.
Area of Science:
- Pathology
- Microbiology
- Critical Care Medicine
Background:
- Meningococcal septicemia is a severe infection with high mortality.
- Understanding its pathogenesis is crucial for developing effective treatments.
Observation:
- Seven fatal cases of meningococcal septicemia were analyzed.
- Morphologic and clinical findings were correlated with experimental data.
Findings:
- Two distinct pathogenetic mechanisms were identified: pulmonary microvascular thrombosis and disseminated intravascular coagulation.
- Pulmonary thrombosis leads to cor pulmonale, unresponsive to heparin.
- Disseminated intravascular coagulation causes adrenal and renal infarction, partially manageable with heparin, but without improving survival.
Implications:
- Current understanding of meningococcal septicemia pathogenesis is incomplete.
- Heparin therapy does not improve survival despite modifying some aspects of the disease.
- Further research is needed to target the primary life-threatening mechanisms.
Related Concept Videos
Rocky Mountain Spotted Fever
Bacterial Meningitis
Viral Meningitis
Cryptococcal Meningitis
Bacterial Meningitis I: Introduction
Bacterial Meningitis II: Pathophysiology

